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 Nerve & Muscle physiology Question & Answer by Dr Khaled A Abulfadle

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مُساهمةموضوع: Nerve & Muscle physiology Question & Answer by Dr Khaled A Abulfadle   الخميس نوفمبر 05, 2015 5:43 am

Q: What do you mean by resting membrane potential is -70 mV?

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A: This means that the potential difference under resting condition between inside and outside the cell membrane is 70 mV with inside relatively negative to outside.




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مُساهمةموضوع: رد: Nerve & Muscle physiology Question & Answer by Dr Khaled A Abulfadle   الأربعاء مايو 04, 2016 7:30 pm

What are the characters of a nerve impulse?
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Answer:




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مُساهمةموضوع: رد: Nerve & Muscle physiology Question & Answer by Dr Khaled A Abulfadle   الخميس مايو 11, 2017 12:51 pm

Q: Vermicular contraction
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A: Vermicular contraction is characterized by being sluggish and lingering contraction. The presence of the vermicular contraction might be a sign of injury of the peripheral nervous system. So, it is contraction of denervated muscle

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مُساهمةموضوع: رد: Nerve & Muscle physiology Question & Answer by Dr Khaled A Abulfadle   الخميس أكتوبر 12, 2017 9:52 am

Q: What is chronaxie, rheobase. Mention the clinincal importance of chronaxie


A: -Chronaxie is the minimum time required for an electric current double the strength of the rheobase to stimulate a muscle or a neuron.
-Rheobase is the lowest intensity with indefinite pulse duration which just stimulated muscles or nerves.
-Chronaxie is dependent on the density of voltage-gated sodium channels in the cell, which affect that cell excitability. It varies across different types of tissue: fast-twitch muscles have a lower chronaxie, slow-twitch muscles have a higher one.
-Chronaxie is the tissue-excitability parameter that permits choice of the optimum stimulus pulse duration for stimulation of any excitable tissue.


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مُساهمةموضوع: رد: Nerve & Muscle physiology Question & Answer by Dr Khaled A Abulfadle   الأحد ديسمبر 10, 2017 9:48 am

Question: Explain why there is a high density of mitochondria in motor end plate
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Answer: There is a high density of mitochondria in motor end plate as the skeletal muscle cells are very active and require a lot of energy.
Also, Mitochondria contribute to neuronal function not only via their ability to generate ATP, but also
via their ability to buffer large Ca2+ loads
When action potentials invade motor nerve terminals, much of the
Ca2+ that enters is temporarily sequestered by mitochondria



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مُساهمةموضوع: رد: Nerve & Muscle physiology Question & Answer by Dr Khaled A Abulfadle   الأحد يناير 28, 2018 5:12 pm

Question
Why the accumulation of lactic acid lead to muscle fatigue ?
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Answer
Very little lactic acid is produced in the muscles at rest and during very mild exercise and that which is produced can be removed quite readily so no excess accumulation occurs. However, when the production rate is high, as it usually is during most athletic contests, the mechanisms for removing lactic acid will be stressed to the limit and become incapable of removing all that is produced. This results in the accumulation of excess lactic acid in the muscles. As lactic acid accumulates in working muscles, their (the muscle’s) pH, which is normally slightly alkaline (7.04), will be reduced to some acidic value between 6.9 and 6.4 . When this happens, a condition called acidosis exists.
As acidosis progressed in muscles it supposedly slowed their contraction force and velocity so that their power output was reduced and athletes were no longer able to maintain a desired level of performance. Supposedly acidosis inhibits the activity of two rate limiting enzymes of metabolism, phosphorylase, which is involved in glycogenolysis), and phosphofructokinase (PFK). In addition, acidosis is thought to interfere with the release of calcium from the sarcoplasmic reticulum, which, in turn, reduces the amount that can bind with troponin on the actin molecule. This binding of calcium with troponin is believed to initiate muscular contraction by allowing the myosin cross bridges to bind with actin and exert an inward pull. Therefore, acidosis could conceivably reduce the contraction force of muscle fibers by both slowing the rate of ATP regeneration and by reducing the number and/or rate of formation of strong bonds between myosin and actin.

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